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Heavy-resistance exercise utilizing very short rest periods is commonly used by body builders to prepare for competition. The purpose of this study was to compare the acute responses of this type of heavy-resistance exercise protocol in competitive body builders (BB) and power lifters (PL). Nine male BB and eight PL were matched for age, size and experience. A ten-station heavy-resistance exercise protocol was used. Each subject performed three sets of 10 repetition maximum (RM) with 10-s rest between sets and alternated 30-s and 60-s rest periods between exercises. No differences were observed in total work between the groups, but BB used a significantly (P less than 0.05) higher percentage of their 1 RM in the bench press and leg press exercises. Heart rate, ratings of perceived exertion (RPE), and lactate levels were obtained during the exercise protocol; significant (P less than 0.05) increases were observed above rest for these variables. RPE was significantly correlated with lactate levels (r = 0.84). Plasma epinephrine, norepinephrine, dopamine, cortisol, and lactate levels significantly increased from pre- to 5 min post-exercise. Mean plasma volumes were reduced -16.6 (+/- 3.64)% and -20.6 (+/- 8.32)% following the exercise protocol for BB and PL, respectively. Significant (P less than 0.05) decreases in eosinophil counts were observed following exercise. No significant differences were observed between BB and PL for any of the physiologic responses measured. PL exhibited a higher incidence (100%) of clinical symptoms of dizziness and nausea compared to BB (11.1%).(ABSTRACT TRUNCATED AT 250 WORDS)

The level of the obese gene product leptin is often positively correlated with body weight, supporting the notion that hyperleptinemia contributes to obesityassociated cardiac dysfunction. However, a link between leptin levels and cardiac function has not been elucidated. This study was designed to examine the role of leptin deficiency (resulting from a point mutation of the leptin gene) in cardiomyocyte contractile function. Mechanical properties and intracellular Ca 2+ transients were evaluated in ventricular myocytes from lean control and leptin-deficient ob/ob obese mice at 12 weeks of age. Cardiac ultrastructure was evaluated using transmission electron microscopy. ob/ob mice were overtly obese, hyperinsulinemic, hypertriglycemic, hypoleptinemic and euglycemic. Ultrastructural examination revealed swelling and disorganization of cristae in mitochondria from ob/ob mouse ventricular tissues. Cardiomyocytes from ob/ob mice displayed reduced expression of the leptin receptor Ob-R, larger cross-sectional area, decreased peak shortening and maximal velocity of shortening/relengthening, and prolonged relengthening but not shortening duration compared with lean counterparts. Consistent with mechanical characteristics, myocytes from ob/ob mice displayed reduced intracellular Ca 2+ release upon electrical stimulus associated with a slowed intracellular Ca 2+ decay rate. Interestingly, the contractile aberrations seen in ob/ob myocytes were significantly improved by in vitro leptin incubation. Contractile dysfunction was not seen in age-and gender-matched high fat-induced obese mice. These results suggested that leptin deficiency contributes to cardiac contractile dysfunction characterized by both systolic and diastolic dysfunction, impaired intracellular Ca 2+ hemostasis and ultrastructural derangement in ventricular myocytes.

Iron deficiency is associated with multiple health problems, including the cardiovascular system. However, the mechanism of action of iron-deficiency-induced cardiovascular damage is unclear. The aim of the present study was to examine the effect of dietary iron deficiency on cardiac ultrastructure, mitochondrial cytochrome c release, NOS (nitric oxide synthase) and several stress-related protein molecules, including protein nitrotyrosine, the p47phox subunit of NADPH oxidase, caveolin-1 and RhoA. Male weanling rats were fed with either control or iron-deficient diets for 12 weeks. Cardiac ultrastructure was examined by transmission electron microscopy. Western blot analysis was used to evaluate cytochrome c, endothelial and inducible NOS, NADPH oxidase, caveolin-1 and RhoA. Protein nitrotyrosine formation was measured by ELISA. Rats fed an iron-deficient diet exhibited increased heart weight and size compared with the control group. Heart width, length and ventricular free wall thickness were similar between the two groups. However, the left ventricular dimension and chamber volume were significantly enhanced in the iron-deficient group compared with controls. Ultrastructural examination revealed mitochondrial swelling and abnormal sarcomere structure in iron-deficient ventricular tissues. Cytochrome c release was significantly enhanced in iron-deficient rats. Protein expression of eNOS (endothelial NOS) and iNOS (inducible NOS), and protein nitrotyrosine formation were significantly elevated in cardiac tissue or mitochondrial extraction from the iron-deficient group. Significantly up-regulated NADPH oxidase, caveolin-1 and RhoA expression were also detected in ventricular tissue of the iron-deficient group. Taken together, these results suggest that dietary iron deficiency may have induced cardiac hypertrophy characterized by aberrant mitochondrial and irregular sarcomere organization, which was accompanied by increased reactive nitrogen species and RhoA expression.

Objective-Vascular smooth muscle cell (VSMC) migration, proliferation, and collagen synthesis are key events involved in the pathogenesis of cardiovascular disease. Growth factors, such as platelet-derived growth factor (PDGF) and fibroblast growth factor, released during vascular injury plays a pivotal role in regulating these events. Curcumin (diferuloyl methane), a major component of the spice turmeric (Curcuma longa), has been shown recently to have beneficial effects in chronic conditions, such as inflammation, cancer, cystic fibrosis, and Alzheimer's disease. The objective of this study was to investigate the ability of curcumin to inhibit PDGF-stimulated migration, proliferation, and collagen synthesis in cultured VSMCs and neointima formation after carotid artery injury in rats. Methods and Results-Curcumin (1 to 25 M) produced a concentration-dependent inhibition of PDGF-elicited VSMC migration, proliferation, and collagen synthesis assessed by chemotaxis, [ 3 H]thymidine incorporation, and [ 3 H]-L-proline incorporation, respectively. Curcumin blocked PDGF-induced VSMC actin-cytoskeleton reorganization, attenuated PDGF signal transduction, and inhibited the binding of PDGF to its receptors. Carotid artery neointima formation was significantly attenuated by perivascular curcumin compared with vehicle controls 14 days after injury, characterized by reduced DNA synthesis, collagen synthesis, and PDGF receptor phosphorylation. Conclusions-These data suggest that curcumin is a potent inhibitor of key PDGF-stimulated VSMC functions and may play a critical role in regulating these events after vascular injury. T he primary event in the development of atherosclerosis and restenosis after percutaneous transluminal coronary angioplasty is thought to involve injury to the endothelium, leading to a response that may be similar to wound healing requiring migration of vascular smooth muscle cells (VSMCs) from the media to the intima and subsequent proliferation. [1][2][3] Intimal smooth muscle cells (SMCs) in the intima assume a synthetic phenotype vis-à-vis the normal contractile phenotype, resulting in the deposition of extracellular matrix within the neointimal tissue. 1,2 Although the mechanisms responsible for migration and proliferation of VSMCs are not fully understood, several factors produced in response to vascular injury have been implicated in this process. 3 Platelet-derived growth factor (PDGF) is a potent growth factor produced by platelets, VSMCs, and endothelial cells in the injured vascular wall. 4,5 PDGF initiates a multitude of biological effects through the activation of intracellular signal transduction pathways that contribute to VSMC proliferation, migration, and collagen synthesis. 6 The importance of PDGF in the development of neointima has been established in arterial injury models. 6 PDGF is also a potent stimulant of extracellular matrix synthesis by VSMCs. Accordingly, inhibition of PDGF-stimulated VSMC migration, proliferation, and extracellular matrix synthesis represents an important...